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Regional 1 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

How many nodes of Ranvier do you have to block to say you have a Block? And what type of conduction have you blocked?

A

3, Saltutory Conduction

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2
Q

If you breach the endoneurium for how long can you have numbness for?

A

4-6 months

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3
Q

Local Anesthetics are what?

A

Drugs that REVERSIBLY block the conduction of electrical impulses along nerve fibers

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4
Q

What influence their ability to produce systemic effects and possibly toxicity?

A

The intrinsic potency and fate of the drugs after absorption

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5
Q

Symptoms of toxicity can occur if administered how?

A

Local infiltration, intravenously or regionally. Pretty much any mode of administration may cause toxicity

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6
Q

Axon?

A

an extension of a centrally located neuron, it is the functional unit of peripheral nerves

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7
Q

Axolemma?

A

also known as Axoplasm, are the intracellular contents and are the major components of the axon

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8
Q

Schwann Cells?

A

It surrounds each axon and functions as support and insulation

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9
Q

Myelin

A

concentric layers of liquid substance in Schwann cells

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10
Q

Nodes of Ranvier

A

Small segments of nerve between Schwann Cells that do not contain myelin

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11
Q

On the Nerve which is the primary site at which LA exert their Action? and why?

A

Nodes of Ranvier; they have limited diffusion barriers for drugs to penetrate, they also contain large numbers of NA+ Channels

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12
Q

What is Saltatory Conduction?

A

Between Nodes of Ranvier where there are large numbers of sodium Channels and are able to generate an action potential so intense that it can jump from node to node; SIGNIFICANTLY FACILITATES CONDUCTION SPEED ALONG THE AXON

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13
Q

Which is harder to block myelinated nerves or unmyelenated nerves? and why?

A

Myelinated Nerves because they are better insulated and are larger, they conduct impulses faster

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14
Q

Fasciculi

A

Bundles of axons

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15
Q

LA must diffuse into what 3 connective tissue layers of the nerve for it to exert their pharmacologic action?

A

Endoneurium, Perineurium, and Epineurium

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16
Q

What is the Resting Membrane potential for neuronal membrane?

A

-70 to -90mV

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17
Q

Where is the Sodium Potassium pump located? and what does it do for membrane potential?

A

It is an active energy dependent process that create the resting Membrane Potential. It keeps a higher concentration of sodium ions outside the cell and a higher concentration of potassium ions inside the cell creating the voltage difference.

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18
Q

Name the 3 functional states of Sodium channels

A

Resting (closed), Open, and inactive

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19
Q

Which channel does the LA bind to?

A

Fast voltage-gated sodium channels within the axon. It prevents the sodium from rushing into the axon.

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20
Q

What does the ionized vs. unionized parts do on the nerve?

A

ionized form binds to the gated sodium channel while in the inactivated state and unionized form crossess the lipid bilayer to enter the neuron.

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21
Q

Cmin is what?

A

Minimum Blocking Concentration; its the lowest concentration of drug that is needed for blocking impulse propagation

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22
Q

what factors determine Cmin?

A

Temp, pH, Ca++ concentration of bathing solution, type of nerve being studied, site of action, dilution, systemic absorption, and degredation

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23
Q

Cmin is analogous to what other anesthetic parameter?

A

Minimal Alveolar Concentration (MAC)

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24
Q

What structure of LA is interchangeable with Ester or Amide?

A

Intermediate bond

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25
Q

What are the 2 Types of LA?

A

Esters and Amide

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26
Q

What correlates with LA POTENCY?

A

Lipid solubility

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27
Q

What correlates with LA DURATION?

A

Protein binding

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28
Q

LA Onset of Action is INDIRECTLY correlated to what?

A

ionization of the LA

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29
Q

Which LA has a faster onset? a more ionized or unionized LA?

A

unionized; it crosses the lipid bilayer to produce LA effect.

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30
Q

3 LA that produces vasoconstriction?

A

Cocaine, Ropivacaine, and Lidocaine

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31
Q

Which 2 vasoconstrictive LA can be administered parentarally?

A

Lidocaine and Ropivacaine

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32
Q

How does Cocaine produce vasoconstrictive properties?

A

it blocks the reuptake of norepinephrine

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33
Q

What determines the peak plasma concentration?

A

Total dose NOT volume or Concentration

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34
Q

2 reasons Epinephrine is used with LA as an additive? What Epi concentration is normally used with LA?

A

Constricts vessels to reduce rate of vascular absorption and serves as marker for intravscular injections.
1:200,000 or 5mcg/ml

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35
Q

What are other additives other then Epinephrine that can be used in LA?

A

opioids, NaHCO3, ketorlac, hyaluronidase

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36
Q

Why are LA combined with NaHCO3?

A

LA are stored more acidic environment making the drug more ionized when administered into a patient acid + base= ionized. But by adding the bicarb it makes the LA more unionized when administered because base + base= unionized

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37
Q

In general what increases absorption of LA?

A

Tissue sites with increased Blood flow increase absorption.

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38
Q

Order of highest uptake to lowest uptake of LA

A

IV, Tracheal, Intercostal, Caudal, Paracervical, Epidural, Brachial plexus, Subarachnoid, Sciatc, Femoral, Subcutaneous
In Time I Can Please Everyone But Susie and Sally

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39
Q

How does Ion trapping Occur?

A

LA overdose leads to Acidosis which increases ionization of the LA that prevents LA from crossing BBB trapping LA in Cerebral Cirulation

40
Q

Ion Trapping in pregnancy

A

LA in maternal circulation and enters the fetus and equilibriates. Because fetus has a lower pH than mom LA becomes more ionized and unable to cross the placenta causing ion trapping

41
Q

why is LA prepared slightly acidic?

A

improves the stability of the drug by increasing the concentration of the ionizedform of drug; when drugs sit unionized for a long period of time it will cause precipitate.

42
Q

Weak acids want to unite with what ions?

A

positively charged ions: Na+ Mg++ or Ca++

43
Q

Weak Bases unite with what ions?

A

Negatively charged ion; Cl- or SO4–

44
Q

What drugs are weak acids?

A

Thiopental and other Barbiturate

45
Q

Acid+Acid=

A

unionized

46
Q

The more unionized a drug is it is easier? or harder? to cross the BBB and the Placenta?

A

easier

47
Q

weak acids give up what?

A

Hydrogen ions

48
Q

Will induction with sodium thiopental be faster if the patient is acidotic or alkalotic?

A

acidotic

49
Q

Should you mix thiopental with a low pH solution?

A

No it may precipitate

50
Q

Why is thiopental mixed and stored in a solution with pH=10-11?

A

Because it is a weak acid and by storing it in a basic solution it makes the drug more ionized decreasing the risk of precipitation of the drug

51
Q

Arm to brain time is how long?

A

28-32 Sec

52
Q

Base+Base=

A

more unionized

53
Q

Acid+Baes

A

more ioniozed

54
Q

Drugs that are weak bases?

A

Ketamine, opioids, and benzodiazepines

55
Q

How are Ester LA metabolized?

A

By ester hydrolysis, Occurs through acions of esterase in plasma, red blood cells, and the liver.
*PRIMARY- plasma choinesterase (rapidly metabolizes ester LA)

56
Q

Other names for plasma Cholinesterase

A

Pseudocholinesterase and Butyrlcholinesterase

57
Q

How are Amide LA metabolized?

A

Primarily by the liver by microsomal cytochrome P-450

58
Q

Which is the least toxic amide LA? but what adverse effect can it cause?

A

Prilocaine clearance is 2.84L/min but it can cause methemoglobinemia

59
Q

What main factors determine rate of elimination for amide metabolism?

A

Hepatic enzyme activity and blood flow

60
Q

What is the most common cause of Local Anesthetic systemic Toxicity (LAST)?

A

The inadvertent intravascular injection and adminstration of excessive dose

61
Q

What effect does LA have on the brain?

A

depression of neuronal function

62
Q

Stimulatory activity in the CNS results from overdose of LA because?

A

LA selectively depresses inhibitory functions in the cerebral cortex letting the facilitory neurons functions go unopposed

63
Q

If you have significant increase of LA in the Plasma what happens to the inhibitory and facilitory pathways?

A

They both get depressed causing generalized CNS depression

64
Q

At what plasma level Concentration do you start seeing toxicity from LA?

A

5mcg/mL ; light headedness, tinnitus, cicumoral and tongue numbness

65
Q

at 5 - 10mcg/mL what toxicity effects do you see from LA?

A

visual disturbance and Muscular twitching

66
Q

at 10-15mcg/mL what toxicity effects do you see from LA?

A

convulsion and unconsiousness

67
Q

at 15 -20mcg/ml what toxicity effects do you see from LA?

A

Coma

68
Q

at 20-25mcg/mL what toxicity effects do you see with LA?

A

Respiratory arrest then CVS depression

69
Q

What happens to PVS in low plasma toxic concentrations LA?

A

vasocontriction

70
Q

What happens to SVR @ high plasma toxic concentrations of LA?

A

Vasodilation leading to hypotension

71
Q

What happens to EKG with CV toxicity from LA?

A

Prolonged conduction time causing AV block, sinus brady, or cardiac arrest

72
Q

Conductivity, automaticity, and pacing of the heart are affected in LA toxicity because?

A

Sodium Channels are blocked

73
Q

Which is more cardio toxic? Bupivacaine or Ropivacaine?

A

Bupivacaine

74
Q

What is the preservative in Amide?

A

Methylparaben

75
Q

What is the preservative in Esters?

A

Para-Aminobenzoic Acid (PABA)

76
Q

Which LA is more likely to have allergic reactions? and why?

A

Esters because of the PABA

77
Q

Why does MetHgb happen when prilocaine or cetacaine is used?

A

they metabolize into O-toluidine which oxidizes Hgb and MetHgb

78
Q

S/S of MetHgb?

A

brownish gray cyanosis, tachypnea and acidosis

79
Q

How do you treat MetHgb?

A

Spontaneous reversal occurs within 2-3hrs. Or can administer Methylene Blue 1mg/kg it immediately reverses the MetHgb.

80
Q

What pt population should you be vigilant in detecting Met Hgb and why?

A

Pt with sever anemia or heart failure because they can’t tolerate decrease O2 carrying capacity

81
Q

What pt population should you avoid MetHgb causing agents?

A

OB patients because 10%conversion of

FHgb to MetHgb leades to fetal cyanosis

82
Q

How to prevent LAST

A
  • ID patients at high risk
  • Pretreat with benzodiazepine 5-10min prior to LA
  • Know Toxic LA limits
  • Monitoring and having resuscitative drugs ready
  • Equipment
  • Aspirate frequently
  • Don’t burn bridge of Communication
83
Q

Treatment of LAST

A
  • Bolus 20% intralipid 1.5ml/kg over 1min then continuous infusion 0.25ml/kg/min.
  • Double the infusion rate if BP returns but remains low
  • Continue the infusion for a minimum of 30min
84
Q

EMLA cream should not be used in what pts?

A

<12 mos age

85
Q

What is EMLA 5% cream composed of?

A

Lidocaine 25mg and Priolocaine 25mg

86
Q

Where should you not inject Epinephrine?

A

fingers, nose, toes, and hose

87
Q

Remember Lidocaine 2345678

A

234g/mol
56% Protein Bound
pKa: 7.8

88
Q

Esters LA are derivatives of what acid?

A

carboxylic acid

89
Q

Is normal Hgb Fe++ or Fe+++?

A

Fe++

90
Q

Fe+++ is what?

A

It is methemoglobin and can’t bind to oxygen

91
Q

Bupivacaine pKa and toxic dose?

A

pKa: 8.1

  1. 5mg/kg w/o epi
  2. 2mg/kg w/epi
92
Q

Lidocaine pKa and toxic dose

A

pKa: 7.8
4mg/kg w/o epi
7mg/kg w/ epi

93
Q

Mepivacaine pKa and toxic dose

A

pKa:7.6
4mg/kg w/o epi
7mg/kg w/ epi

94
Q

Ropivacaine pKa and toxic dose

A

pKa: 8.1
3mg/kg w/o epi
3.5mg/kg w/ epi

95
Q

What can you do when pt is allergic to and ester? when pt is unresponsive to epi and steroids?

A

Can give Methylene Blue

Regional 1 (2 decks)

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